About 3.3 billion people—half of the world's population—are at risk of malaria. In the year 2012, this led to about 207 million malaria cases and approx. 627,000 deaths (World Health Organization 2013). Malaria is especially a serious problem in Africa, where one in every five (20%) childhood deaths is due to the effects of the disease. An African child has on average between 1.6 and 5.4 episodes of malaria fever each year.
Malarial diseases in humans are caused by five species of the Plasmodium parasite: P. falciparum (causing Malaria tropica), P. vivax (causing Malaria tertiana), P. ovale (causing Malaria tertiana), P. knowlesi (causing Malaria quotidiana) and P. malariae (causing Malaria quartana). Each of these species is transmitted to the human via female Anopheles mosquitoes that transmit Plasmodium parasites in the stage of sporozoites. Once the sporozoites enter the bloodstream of the human, they localize in liver cells, i.e. hepatocytes. One to two weeks later, the infected hepatocytes rupture and release merosomes. These merosomes circulate in the blood stream for short time before releasing merozoites. These then begin the erythrocytic phase of malaria by attaching to and invading red blood cells, or erythrocytes. The erythrocytic stage of the life cycle begins, which is the direct cause of malarial pathogenesis and pathology. The fever, anemia, circulatory changes, and immunopathologic phenomena characteristic of malaria are largely the result of red cell rupture and the host's immune response to parasite antigen and hemozoin. For these reasons, the erythrocytic stage of the Plasmodium life cycle is of vital importance to passive or active vaccine development and treatment of malaria.
Malaria caused by Plasmodium falciparum (also called malignant malaria, falciparum malaria or malaria tropica) is the most dangerous form of malaria, with the highest rates of complications and mortality. Almost all malarial deaths are caused by P. falciparum. 
Resistance of Plasmodium falciparum to the existing anti-malarial drug chloroquine emerged in the sixties of the last century in asia and has spread worldwide since then. In addition, the malaria parasite has developed resistance to most other anti-malarial drugs over the past decade. This poses a major threat to public health. There is every reason to believe that the prevalence and degree of anti-malarial drug resistance will continue to increase. Furthermore, many anti-malaria drugs have been notorious for their toxic side effects, e. g. mefloquin. Today, the recommended treatments against Plasmodium falciparum malaria are artemisinin-based combination therapies. But also against this therapy, resistances start to occur in different parts of the world, e.g. Kenya and Cambodia (Borrmann et al. 2011; Noedl, Socheat, and Satimai 2009).
In principle, antibodies against Plasmodium falciparum with appropriate specificity and activity are desirable as an anti-malaria drug. Human antibodies would be advantageous over non-human antibodies and humanized, chimeric antibodies for use in human therapy for several reasons: A human antibody is less likely to induce an immunological response in humans than antibodies that contain non-human portions. This immune response against non-human portions rules out the possibility of repeated therapies with such antibodies. In conclusion, human antibodies can be used multiple times as a treatment regimen. Furthermore, a human antibody is less likely to be recognized as a “foreign” antibody in humans. This will result in neutralization or slower elimination of the human antibody from the body than a non-human or partially human antibody. Accordingly, a human antibody can be administered at lower doses or the treatment regimen can be adapted to lower frequency than non-human or partially human antibodies.
Therefore the availability of novel human antibodies to inhibit the growth and/or invasion of Plasmodium parasites, in particular for the treatment of malaria infected individuals, would be highly advantageous.